Iron Restriction

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Hisashi Sawada - One of the best experts on this subject based on the ideXlab platform.

  • Influence of dietary Iron intake Restriction on the development of hypertension in weanling prehypertensive rats
    Heart and Vessels, 2018
    Co-Authors: Keisuke Okuno, Yoshiro Naito, Hisashi Sawada, Makiko Oboshi, Koichi Nishimura, Seiki Yasumura, Masanori Asakura, Masaharu Ishihara, Tohru Masuyama
    Abstract:

    Hypertension is a major public health problem leading to death. To reduce the morbidity and mortality in patients with hypertension, it is crucial to develop a novel strategy for prevention of hypertension. We have currently reported an attempt at dietary Iron intake Restriction as non-pharmacological treatment of hypertension in patients with hypertension. However, it remains fully unknown whether dietary Iron Restriction prevents the development of hypertension. We investigated the influence of dietary Iron Restriction on the development of hypertension in weanling pre-hypertensive model rats. 3-week-old male stroke-prone spontaneously hypertensive rats (SHR-SP) were randomly divided into two groups and were given an ad libitum normal diet or an Iron-restricted diet for 12 weeks. Blood pressure was progressively increased in SHR-SP according to growth, while dietary Iron Restriction attenuated the development of hypertension. Proteinuria was also increased in SHR-SP according to growth, whereas dietary Iron Restriction suppressed the increment of proteinuria. SHR-SP exhibited glomerulosclerosis and exacerbated renal interstitial fibrosis at 15 weeks old, indicating that SHR-SP developed hypertensive nephropathy in the adult stage; however, these changes were attenuated by dietary Iron Restriction. Gelatin zymography showed dietary Iron Restriction decreased both renal MMP-2 and MMP-9 activities in SHR-SP at 15 weeks old. Of interest, dietary Iron Restriction suppressed renal TGFβ-RI expression and Smad2 phosphorylation in SHR-SP. Furthermore, dietary Iron Restriction decreased renal fibrosis, renal MMP-2 and MMP-9 activities, renal TGFβ-RI expression, and Smad2 phosphorylation in rats with unilateral ureteral obstruction. Dietary Iron Restriction prevented the development of hypertension in weanling pre-hypertensive rats.

  • Iron-restricted pair-feeding affects renal damage in rats with chronic kidney disease.
    PloS one, 2017
    Co-Authors: Yoshiro Naito, Hisashi Sawada, Makiko Oboshi, Keisuke Okuno, Seiki Yasumura, Masaharu Ishihara, Aya Senchi, Tetsuo Horimatsu, Tohru Masuyama
    Abstract:

    Background We have previously shown that dietary Iron Restriction prevents the development of renal damage in a rat model of chronic kidney disease (CKD). However, Iron deficiency is associated with appetite loss. In addition, calorie Restriction is reported to prevent the development of end-stage renal pathology in CKD rats. Thus, the beneficial effect of Iron Restriction on renal damage may depend on calorie Restriction. Here, we investigate the effect of pair-feeding Iron Restriction on renal damage in a rat model of CKD. Methods First, to determine the amount of food intake, Sprague-Dawley (SD) rats were randomly given an ad libitum normal diet or an Iron-restricted diet, and the food intake was measured. Second, CKD was induced by a 5/6 nephrectomy in SD rats, and CKD rats were given either a pair-feeding normal or Iron-restricted diet. Results Food intake was reduced in the Iron-restricted diet group compared to the normal diet group of SD rats for 16 weeks (mean food intake; normal diet group and Iron-restricted diet group: 25 and 20 g/day, respectively). Based on the initial experiments, CKD rats received either a pair-feeding normal or Iron-restricted diet (20 g/day) for 16 weeks. Importantly, pair-feeding Iron Restriction prevented the development of proteinuria, glomerulosclerosis, and tubulointerstitial damage in CKD rats. Interestingly, pair-feeding Iron Restriction attenuated renal expression of nuclear mineralocorticoid receptor in CKD rats. Conclusions Pair-feeding Iron Restriction affected renal damage in a rat model of CKD.

  • Attenuation of hypertension and renal damage in renovascular hypertensive rats by Iron Restriction
    Hypertension Research, 2016
    Co-Authors: Makiko Oboshi, Yoshiro Naito, Hisashi Sawada, Shinichi Hirotani, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Takeshi Tsujino, Toshiaki Mano, Tohru Masuyama
    Abstract:

    Iron is a catalyst in the formation of reactive oxygen species. Oxidative stress is associated with the pathogenesis of both human and experimental animal models of renovascular hypertension. We hypothesized that Iron is involved in the pathogenesis of renovascular hypertension and that Iron Restriction may affect the pathogenesis of renovascular hypertension via the inhibition of oxidative stress. Herein, we investigated the effect of Iron Restriction on hypertension and renal damage in a rat model of two-kidney one-clip (2K1C) renovascular hypertension. Renovascular hypertension was induced by 2K1C in male Sprague–Dawley rats. At the day of clipping, 2K1C rats were divided into untreated (2K1C) and dietary Iron-restricted groups (2K1C+IR). The 2K1C rats showed hypertension after the day of clipping, whereas dietary Iron Restriction attenuated the development of hypertension. Vascular hypertrophy and the increased fibrotic area were suppressed in the 2K1C+IR group. The clipped kidney developed renal atrophy in both the 2K1C and 2K1C+IR groups after clipping. However, the unclipped kidney showed renal hypertrophy in the 2K1C and 2K1C+IR groups, and the extent was less in the 2K1C+IR group. The 2K1C rats exhibited glomerulosclerosis and tubulointerstitial fibrosis in the unclipped kidney, whereas these changes were attenuated by an Iron-restricted diet. Importantly, proteinuria was decreased in the 2K1C+IR group, along with decreased urinary 8-hydroxy-2'-deoxyguanosine excretion and superoxide production of the unclipped kidney. Moreover, the expression of nuclear mineralocorticoid receptor in the unclipped kidney of the 2K1C rats was attenuated by Iron Restriction. These data indicate a novel effect of Iron Restriction on hypertension and renal damage in renovascular hypertension.

  • attenuation of hypertension and renal damage in renovascular hypertensive rats by Iron Restriction
    Hypertension Research, 2016
    Co-Authors: Makiko Oboshi, Yoshiro Naito, Hisashi Sawada, Shinichi Hirotani, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Takeshi Tsujino, Toshiaki Mano, Tohru Masuyama
    Abstract:

    Attenuation of hypertension and renal damage in renovascular hypertensive rats by Iron Restriction

  • Iron is associated with the development of hypoxia-induced pulmonary vascular remodeling in mice.
    Heart and vessels, 2016
    Co-Authors: Yoshiro Naito, Hisashi Sawada, Makiko Oboshi, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Koichi Nishimura, Manami Hosokawa, Yuko Soyama, Shinichi Hirotani
    Abstract:

    Several recent observations provide the association of Iron deficiency with pulmonary hypertension (PH) in human and animal studies. However, it remains completely unknown whether PH leads to Iron deficiency or Iron deficiency enhances the development of PH. In addition, it is obscure whether Iron is associated with the development of pulmonary vascular remodeling in PH. In this study, we investigate the impacts of dietary Iron Restriction on the development of hypoxia-induced pulmonary vascular remodeling in mice. Eight- to ten-week-old male C57BL/6J mice were exposed to chronic hypoxia for 4 weeks. Mice exposed to hypoxia were randomly divided into two groups and were given a normal diet or an Iron-restricted diet. Mice maintained in room air served as normoxic controls. Chronic hypoxia induced pulmonary vascular remodeling, while Iron Restriction led a modest attenuation of this change. In addition, chronic hypoxia exhibited increased RV systolic pressure, which was attenuated by Iron Restriction. Moreover, the increase in RV cardiomyocyte cross-sectional area and RV interstitial fibrosis was observed in mice exposed to chronic hypoxia. In contrast, Iron Restriction suppressed these changes. Consistent with these changes, RV weight to left ventricular + interventricular septum weight ratio was increased in mice exposed to chronic hypoxia, while this increment was inhibited by Iron Restriction. Taken together, these results suggest that Iron is associated with the development of hypoxia-induced pulmonary vascular remodeling in mice.

Yoshiro Naito - One of the best experts on this subject based on the ideXlab platform.

  • Influence of dietary Iron intake Restriction on the development of hypertension in weanling prehypertensive rats
    Heart and Vessels, 2018
    Co-Authors: Keisuke Okuno, Yoshiro Naito, Hisashi Sawada, Makiko Oboshi, Koichi Nishimura, Seiki Yasumura, Masanori Asakura, Masaharu Ishihara, Tohru Masuyama
    Abstract:

    Hypertension is a major public health problem leading to death. To reduce the morbidity and mortality in patients with hypertension, it is crucial to develop a novel strategy for prevention of hypertension. We have currently reported an attempt at dietary Iron intake Restriction as non-pharmacological treatment of hypertension in patients with hypertension. However, it remains fully unknown whether dietary Iron Restriction prevents the development of hypertension. We investigated the influence of dietary Iron Restriction on the development of hypertension in weanling pre-hypertensive model rats. 3-week-old male stroke-prone spontaneously hypertensive rats (SHR-SP) were randomly divided into two groups and were given an ad libitum normal diet or an Iron-restricted diet for 12 weeks. Blood pressure was progressively increased in SHR-SP according to growth, while dietary Iron Restriction attenuated the development of hypertension. Proteinuria was also increased in SHR-SP according to growth, whereas dietary Iron Restriction suppressed the increment of proteinuria. SHR-SP exhibited glomerulosclerosis and exacerbated renal interstitial fibrosis at 15 weeks old, indicating that SHR-SP developed hypertensive nephropathy in the adult stage; however, these changes were attenuated by dietary Iron Restriction. Gelatin zymography showed dietary Iron Restriction decreased both renal MMP-2 and MMP-9 activities in SHR-SP at 15 weeks old. Of interest, dietary Iron Restriction suppressed renal TGFβ-RI expression and Smad2 phosphorylation in SHR-SP. Furthermore, dietary Iron Restriction decreased renal fibrosis, renal MMP-2 and MMP-9 activities, renal TGFβ-RI expression, and Smad2 phosphorylation in rats with unilateral ureteral obstruction. Dietary Iron Restriction prevented the development of hypertension in weanling pre-hypertensive rats.

  • Iron-restricted pair-feeding affects renal damage in rats with chronic kidney disease.
    PloS one, 2017
    Co-Authors: Yoshiro Naito, Hisashi Sawada, Makiko Oboshi, Keisuke Okuno, Seiki Yasumura, Masaharu Ishihara, Aya Senchi, Tetsuo Horimatsu, Tohru Masuyama
    Abstract:

    Background We have previously shown that dietary Iron Restriction prevents the development of renal damage in a rat model of chronic kidney disease (CKD). However, Iron deficiency is associated with appetite loss. In addition, calorie Restriction is reported to prevent the development of end-stage renal pathology in CKD rats. Thus, the beneficial effect of Iron Restriction on renal damage may depend on calorie Restriction. Here, we investigate the effect of pair-feeding Iron Restriction on renal damage in a rat model of CKD. Methods First, to determine the amount of food intake, Sprague-Dawley (SD) rats were randomly given an ad libitum normal diet or an Iron-restricted diet, and the food intake was measured. Second, CKD was induced by a 5/6 nephrectomy in SD rats, and CKD rats were given either a pair-feeding normal or Iron-restricted diet. Results Food intake was reduced in the Iron-restricted diet group compared to the normal diet group of SD rats for 16 weeks (mean food intake; normal diet group and Iron-restricted diet group: 25 and 20 g/day, respectively). Based on the initial experiments, CKD rats received either a pair-feeding normal or Iron-restricted diet (20 g/day) for 16 weeks. Importantly, pair-feeding Iron Restriction prevented the development of proteinuria, glomerulosclerosis, and tubulointerstitial damage in CKD rats. Interestingly, pair-feeding Iron Restriction attenuated renal expression of nuclear mineralocorticoid receptor in CKD rats. Conclusions Pair-feeding Iron Restriction affected renal damage in a rat model of CKD.

  • Attenuation of hypertension and renal damage in renovascular hypertensive rats by Iron Restriction
    Hypertension Research, 2016
    Co-Authors: Makiko Oboshi, Yoshiro Naito, Hisashi Sawada, Shinichi Hirotani, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Takeshi Tsujino, Toshiaki Mano, Tohru Masuyama
    Abstract:

    Iron is a catalyst in the formation of reactive oxygen species. Oxidative stress is associated with the pathogenesis of both human and experimental animal models of renovascular hypertension. We hypothesized that Iron is involved in the pathogenesis of renovascular hypertension and that Iron Restriction may affect the pathogenesis of renovascular hypertension via the inhibition of oxidative stress. Herein, we investigated the effect of Iron Restriction on hypertension and renal damage in a rat model of two-kidney one-clip (2K1C) renovascular hypertension. Renovascular hypertension was induced by 2K1C in male Sprague–Dawley rats. At the day of clipping, 2K1C rats were divided into untreated (2K1C) and dietary Iron-restricted groups (2K1C+IR). The 2K1C rats showed hypertension after the day of clipping, whereas dietary Iron Restriction attenuated the development of hypertension. Vascular hypertrophy and the increased fibrotic area were suppressed in the 2K1C+IR group. The clipped kidney developed renal atrophy in both the 2K1C and 2K1C+IR groups after clipping. However, the unclipped kidney showed renal hypertrophy in the 2K1C and 2K1C+IR groups, and the extent was less in the 2K1C+IR group. The 2K1C rats exhibited glomerulosclerosis and tubulointerstitial fibrosis in the unclipped kidney, whereas these changes were attenuated by an Iron-restricted diet. Importantly, proteinuria was decreased in the 2K1C+IR group, along with decreased urinary 8-hydroxy-2'-deoxyguanosine excretion and superoxide production of the unclipped kidney. Moreover, the expression of nuclear mineralocorticoid receptor in the unclipped kidney of the 2K1C rats was attenuated by Iron Restriction. These data indicate a novel effect of Iron Restriction on hypertension and renal damage in renovascular hypertension.

  • attenuation of hypertension and renal damage in renovascular hypertensive rats by Iron Restriction
    Hypertension Research, 2016
    Co-Authors: Makiko Oboshi, Yoshiro Naito, Hisashi Sawada, Shinichi Hirotani, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Takeshi Tsujino, Toshiaki Mano, Tohru Masuyama
    Abstract:

    Attenuation of hypertension and renal damage in renovascular hypertensive rats by Iron Restriction

  • Iron is associated with the development of hypoxia-induced pulmonary vascular remodeling in mice.
    Heart and vessels, 2016
    Co-Authors: Yoshiro Naito, Hisashi Sawada, Makiko Oboshi, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Koichi Nishimura, Manami Hosokawa, Yuko Soyama, Shinichi Hirotani
    Abstract:

    Several recent observations provide the association of Iron deficiency with pulmonary hypertension (PH) in human and animal studies. However, it remains completely unknown whether PH leads to Iron deficiency or Iron deficiency enhances the development of PH. In addition, it is obscure whether Iron is associated with the development of pulmonary vascular remodeling in PH. In this study, we investigate the impacts of dietary Iron Restriction on the development of hypoxia-induced pulmonary vascular remodeling in mice. Eight- to ten-week-old male C57BL/6J mice were exposed to chronic hypoxia for 4 weeks. Mice exposed to hypoxia were randomly divided into two groups and were given a normal diet or an Iron-restricted diet. Mice maintained in room air served as normoxic controls. Chronic hypoxia induced pulmonary vascular remodeling, while Iron Restriction led a modest attenuation of this change. In addition, chronic hypoxia exhibited increased RV systolic pressure, which was attenuated by Iron Restriction. Moreover, the increase in RV cardiomyocyte cross-sectional area and RV interstitial fibrosis was observed in mice exposed to chronic hypoxia. In contrast, Iron Restriction suppressed these changes. Consistent with these changes, RV weight to left ventricular + interventricular septum weight ratio was increased in mice exposed to chronic hypoxia, while this increment was inhibited by Iron Restriction. Taken together, these results suggest that Iron is associated with the development of hypoxia-induced pulmonary vascular remodeling in mice.

Tohru Masuyama - One of the best experts on this subject based on the ideXlab platform.

  • Influence of dietary Iron intake Restriction on the development of hypertension in weanling prehypertensive rats
    Heart and Vessels, 2018
    Co-Authors: Keisuke Okuno, Yoshiro Naito, Hisashi Sawada, Makiko Oboshi, Koichi Nishimura, Seiki Yasumura, Masanori Asakura, Masaharu Ishihara, Tohru Masuyama
    Abstract:

    Hypertension is a major public health problem leading to death. To reduce the morbidity and mortality in patients with hypertension, it is crucial to develop a novel strategy for prevention of hypertension. We have currently reported an attempt at dietary Iron intake Restriction as non-pharmacological treatment of hypertension in patients with hypertension. However, it remains fully unknown whether dietary Iron Restriction prevents the development of hypertension. We investigated the influence of dietary Iron Restriction on the development of hypertension in weanling pre-hypertensive model rats. 3-week-old male stroke-prone spontaneously hypertensive rats (SHR-SP) were randomly divided into two groups and were given an ad libitum normal diet or an Iron-restricted diet for 12 weeks. Blood pressure was progressively increased in SHR-SP according to growth, while dietary Iron Restriction attenuated the development of hypertension. Proteinuria was also increased in SHR-SP according to growth, whereas dietary Iron Restriction suppressed the increment of proteinuria. SHR-SP exhibited glomerulosclerosis and exacerbated renal interstitial fibrosis at 15 weeks old, indicating that SHR-SP developed hypertensive nephropathy in the adult stage; however, these changes were attenuated by dietary Iron Restriction. Gelatin zymography showed dietary Iron Restriction decreased both renal MMP-2 and MMP-9 activities in SHR-SP at 15 weeks old. Of interest, dietary Iron Restriction suppressed renal TGFβ-RI expression and Smad2 phosphorylation in SHR-SP. Furthermore, dietary Iron Restriction decreased renal fibrosis, renal MMP-2 and MMP-9 activities, renal TGFβ-RI expression, and Smad2 phosphorylation in rats with unilateral ureteral obstruction. Dietary Iron Restriction prevented the development of hypertension in weanling pre-hypertensive rats.

  • Iron-restricted pair-feeding affects renal damage in rats with chronic kidney disease.
    PloS one, 2017
    Co-Authors: Yoshiro Naito, Hisashi Sawada, Makiko Oboshi, Keisuke Okuno, Seiki Yasumura, Masaharu Ishihara, Aya Senchi, Tetsuo Horimatsu, Tohru Masuyama
    Abstract:

    Background We have previously shown that dietary Iron Restriction prevents the development of renal damage in a rat model of chronic kidney disease (CKD). However, Iron deficiency is associated with appetite loss. In addition, calorie Restriction is reported to prevent the development of end-stage renal pathology in CKD rats. Thus, the beneficial effect of Iron Restriction on renal damage may depend on calorie Restriction. Here, we investigate the effect of pair-feeding Iron Restriction on renal damage in a rat model of CKD. Methods First, to determine the amount of food intake, Sprague-Dawley (SD) rats were randomly given an ad libitum normal diet or an Iron-restricted diet, and the food intake was measured. Second, CKD was induced by a 5/6 nephrectomy in SD rats, and CKD rats were given either a pair-feeding normal or Iron-restricted diet. Results Food intake was reduced in the Iron-restricted diet group compared to the normal diet group of SD rats for 16 weeks (mean food intake; normal diet group and Iron-restricted diet group: 25 and 20 g/day, respectively). Based on the initial experiments, CKD rats received either a pair-feeding normal or Iron-restricted diet (20 g/day) for 16 weeks. Importantly, pair-feeding Iron Restriction prevented the development of proteinuria, glomerulosclerosis, and tubulointerstitial damage in CKD rats. Interestingly, pair-feeding Iron Restriction attenuated renal expression of nuclear mineralocorticoid receptor in CKD rats. Conclusions Pair-feeding Iron Restriction affected renal damage in a rat model of CKD.

  • Attenuation of hypertension and renal damage in renovascular hypertensive rats by Iron Restriction
    Hypertension Research, 2016
    Co-Authors: Makiko Oboshi, Yoshiro Naito, Hisashi Sawada, Shinichi Hirotani, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Takeshi Tsujino, Toshiaki Mano, Tohru Masuyama
    Abstract:

    Iron is a catalyst in the formation of reactive oxygen species. Oxidative stress is associated with the pathogenesis of both human and experimental animal models of renovascular hypertension. We hypothesized that Iron is involved in the pathogenesis of renovascular hypertension and that Iron Restriction may affect the pathogenesis of renovascular hypertension via the inhibition of oxidative stress. Herein, we investigated the effect of Iron Restriction on hypertension and renal damage in a rat model of two-kidney one-clip (2K1C) renovascular hypertension. Renovascular hypertension was induced by 2K1C in male Sprague–Dawley rats. At the day of clipping, 2K1C rats were divided into untreated (2K1C) and dietary Iron-restricted groups (2K1C+IR). The 2K1C rats showed hypertension after the day of clipping, whereas dietary Iron Restriction attenuated the development of hypertension. Vascular hypertrophy and the increased fibrotic area were suppressed in the 2K1C+IR group. The clipped kidney developed renal atrophy in both the 2K1C and 2K1C+IR groups after clipping. However, the unclipped kidney showed renal hypertrophy in the 2K1C and 2K1C+IR groups, and the extent was less in the 2K1C+IR group. The 2K1C rats exhibited glomerulosclerosis and tubulointerstitial fibrosis in the unclipped kidney, whereas these changes were attenuated by an Iron-restricted diet. Importantly, proteinuria was decreased in the 2K1C+IR group, along with decreased urinary 8-hydroxy-2'-deoxyguanosine excretion and superoxide production of the unclipped kidney. Moreover, the expression of nuclear mineralocorticoid receptor in the unclipped kidney of the 2K1C rats was attenuated by Iron Restriction. These data indicate a novel effect of Iron Restriction on hypertension and renal damage in renovascular hypertension.

  • attenuation of hypertension and renal damage in renovascular hypertensive rats by Iron Restriction
    Hypertension Research, 2016
    Co-Authors: Makiko Oboshi, Yoshiro Naito, Hisashi Sawada, Shinichi Hirotani, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Takeshi Tsujino, Toshiaki Mano, Tohru Masuyama
    Abstract:

    Attenuation of hypertension and renal damage in renovascular hypertensive rats by Iron Restriction

  • Iron Restriction inhibits renal injury in aldosterone/salt-induced hypertensive mice
    Hypertension Research, 2015
    Co-Authors: Hisashi Sawada, Yoshiro Naito, Makiko Oboshi, Shinichi Hirotani, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Daisuke Morisawa, Tohru Masuyama
    Abstract:

    Excess Iron is associated with the pathogenesis of several renal diseases. Aldosterone is reported to have deleterious effects on the kidney, but there have been no reports of the role of Iron in aldosterone/salt-induced renal injury. Therefore, we investigated the effects of dietary Iron Restriction on the development of hypertension and renal injury in aldosterone/salt-induced hypertensive mice. Ten-week-old male C57BL/6J mice were uninephrectomized and infused with aldosterone for four weeks. These were divided into two groups: one fed a high-salt diet (Aldo) and the other fed a high-salt with Iron-restricted diet (Aldo-IR). Vehicle-infused mice without a uninephrectomy were also divided into two groups: one fed a normal diet (control) and the other fed an Iron-restricted diet (IR) for 4 weeks. As compared with control and IR mice, Aldo mice showed an increase in both systolic blood pressure and urinary albumin/creatinine ratio, but these increases were reduced in the Aldo-IR group. In addition, renal histology revealed that Aldo mice exhibited glomerulosclerosis and tubulointerstitial fibrosis, whereas these changes were attenuated in Aldo-IR mice. Expression of intracellular Iron transport protein transferrin receptor 1 was increased in the renal tubules of Aldo mice compared with control mice. Dietary Iron Restriction attenuated the development of hypertension and renal injury in aldosterone/salt-induced hypertensive mice.

Shinichi Hirotani - One of the best experts on this subject based on the ideXlab platform.

  • Attenuation of hypertension and renal damage in renovascular hypertensive rats by Iron Restriction
    Hypertension Research, 2016
    Co-Authors: Makiko Oboshi, Yoshiro Naito, Hisashi Sawada, Shinichi Hirotani, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Takeshi Tsujino, Toshiaki Mano, Tohru Masuyama
    Abstract:

    Iron is a catalyst in the formation of reactive oxygen species. Oxidative stress is associated with the pathogenesis of both human and experimental animal models of renovascular hypertension. We hypothesized that Iron is involved in the pathogenesis of renovascular hypertension and that Iron Restriction may affect the pathogenesis of renovascular hypertension via the inhibition of oxidative stress. Herein, we investigated the effect of Iron Restriction on hypertension and renal damage in a rat model of two-kidney one-clip (2K1C) renovascular hypertension. Renovascular hypertension was induced by 2K1C in male Sprague–Dawley rats. At the day of clipping, 2K1C rats were divided into untreated (2K1C) and dietary Iron-restricted groups (2K1C+IR). The 2K1C rats showed hypertension after the day of clipping, whereas dietary Iron Restriction attenuated the development of hypertension. Vascular hypertrophy and the increased fibrotic area were suppressed in the 2K1C+IR group. The clipped kidney developed renal atrophy in both the 2K1C and 2K1C+IR groups after clipping. However, the unclipped kidney showed renal hypertrophy in the 2K1C and 2K1C+IR groups, and the extent was less in the 2K1C+IR group. The 2K1C rats exhibited glomerulosclerosis and tubulointerstitial fibrosis in the unclipped kidney, whereas these changes were attenuated by an Iron-restricted diet. Importantly, proteinuria was decreased in the 2K1C+IR group, along with decreased urinary 8-hydroxy-2'-deoxyguanosine excretion and superoxide production of the unclipped kidney. Moreover, the expression of nuclear mineralocorticoid receptor in the unclipped kidney of the 2K1C rats was attenuated by Iron Restriction. These data indicate a novel effect of Iron Restriction on hypertension and renal damage in renovascular hypertension.

  • attenuation of hypertension and renal damage in renovascular hypertensive rats by Iron Restriction
    Hypertension Research, 2016
    Co-Authors: Makiko Oboshi, Yoshiro Naito, Hisashi Sawada, Shinichi Hirotani, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Takeshi Tsujino, Toshiaki Mano, Tohru Masuyama
    Abstract:

    Attenuation of hypertension and renal damage in renovascular hypertensive rats by Iron Restriction

  • Iron is associated with the development of hypoxia-induced pulmonary vascular remodeling in mice.
    Heart and vessels, 2016
    Co-Authors: Yoshiro Naito, Hisashi Sawada, Makiko Oboshi, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Koichi Nishimura, Manami Hosokawa, Yuko Soyama, Shinichi Hirotani
    Abstract:

    Several recent observations provide the association of Iron deficiency with pulmonary hypertension (PH) in human and animal studies. However, it remains completely unknown whether PH leads to Iron deficiency or Iron deficiency enhances the development of PH. In addition, it is obscure whether Iron is associated with the development of pulmonary vascular remodeling in PH. In this study, we investigate the impacts of dietary Iron Restriction on the development of hypoxia-induced pulmonary vascular remodeling in mice. Eight- to ten-week-old male C57BL/6J mice were exposed to chronic hypoxia for 4 weeks. Mice exposed to hypoxia were randomly divided into two groups and were given a normal diet or an Iron-restricted diet. Mice maintained in room air served as normoxic controls. Chronic hypoxia induced pulmonary vascular remodeling, while Iron Restriction led a modest attenuation of this change. In addition, chronic hypoxia exhibited increased RV systolic pressure, which was attenuated by Iron Restriction. Moreover, the increase in RV cardiomyocyte cross-sectional area and RV interstitial fibrosis was observed in mice exposed to chronic hypoxia. In contrast, Iron Restriction suppressed these changes. Consistent with these changes, RV weight to left ventricular + interventricular septum weight ratio was increased in mice exposed to chronic hypoxia, while this increment was inhibited by Iron Restriction. Taken together, these results suggest that Iron is associated with the development of hypoxia-induced pulmonary vascular remodeling in mice.

  • Temporary Dietary Iron Restriction Affects the Process of Thrombus Resolution in a Rat Model of Deep Vein Thrombosis
    PloS one, 2015
    Co-Authors: Makiko Oboshi, Yoshiro Naito, Hisashi Sawada, Shinichi Hirotani, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Daisuke Morisawa, Koichi Nishimura, Kenichi Fujii
    Abstract:

    Background Deep vein thrombosis (DVT) is a major cause of pulmonary thromboembolism and sudden death. Thus, it is important to consider the pathophysiology of DVT. Recently, Iron has been reported to be associated with thrombotic diseases. Hence, in this study, we investigate the effects of dietary Iron Restriction on the process of thrombus resolution in a rat model of DVT.

  • Iron Restriction inhibits renal injury in aldosterone/salt-induced hypertensive mice
    Hypertension Research, 2015
    Co-Authors: Hisashi Sawada, Yoshiro Naito, Makiko Oboshi, Shinichi Hirotani, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Daisuke Morisawa, Tohru Masuyama
    Abstract:

    Excess Iron is associated with the pathogenesis of several renal diseases. Aldosterone is reported to have deleterious effects on the kidney, but there have been no reports of the role of Iron in aldosterone/salt-induced renal injury. Therefore, we investigated the effects of dietary Iron Restriction on the development of hypertension and renal injury in aldosterone/salt-induced hypertensive mice. Ten-week-old male C57BL/6J mice were uninephrectomized and infused with aldosterone for four weeks. These were divided into two groups: one fed a high-salt diet (Aldo) and the other fed a high-salt with Iron-restricted diet (Aldo-IR). Vehicle-infused mice without a uninephrectomy were also divided into two groups: one fed a normal diet (control) and the other fed an Iron-restricted diet (IR) for 4 weeks. As compared with control and IR mice, Aldo mice showed an increase in both systolic blood pressure and urinary albumin/creatinine ratio, but these increases were reduced in the Aldo-IR group. In addition, renal histology revealed that Aldo mice exhibited glomerulosclerosis and tubulointerstitial fibrosis, whereas these changes were attenuated in Aldo-IR mice. Expression of intracellular Iron transport protein transferrin receptor 1 was increased in the renal tubules of Aldo mice compared with control mice. Dietary Iron Restriction attenuated the development of hypertension and renal injury in aldosterone/salt-induced hypertensive mice.

Akiyo Eguchi - One of the best experts on this subject based on the ideXlab platform.

  • Attenuation of hypertension and renal damage in renovascular hypertensive rats by Iron Restriction
    Hypertension Research, 2016
    Co-Authors: Makiko Oboshi, Yoshiro Naito, Hisashi Sawada, Shinichi Hirotani, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Takeshi Tsujino, Toshiaki Mano, Tohru Masuyama
    Abstract:

    Iron is a catalyst in the formation of reactive oxygen species. Oxidative stress is associated with the pathogenesis of both human and experimental animal models of renovascular hypertension. We hypothesized that Iron is involved in the pathogenesis of renovascular hypertension and that Iron Restriction may affect the pathogenesis of renovascular hypertension via the inhibition of oxidative stress. Herein, we investigated the effect of Iron Restriction on hypertension and renal damage in a rat model of two-kidney one-clip (2K1C) renovascular hypertension. Renovascular hypertension was induced by 2K1C in male Sprague–Dawley rats. At the day of clipping, 2K1C rats were divided into untreated (2K1C) and dietary Iron-restricted groups (2K1C+IR). The 2K1C rats showed hypertension after the day of clipping, whereas dietary Iron Restriction attenuated the development of hypertension. Vascular hypertrophy and the increased fibrotic area were suppressed in the 2K1C+IR group. The clipped kidney developed renal atrophy in both the 2K1C and 2K1C+IR groups after clipping. However, the unclipped kidney showed renal hypertrophy in the 2K1C and 2K1C+IR groups, and the extent was less in the 2K1C+IR group. The 2K1C rats exhibited glomerulosclerosis and tubulointerstitial fibrosis in the unclipped kidney, whereas these changes were attenuated by an Iron-restricted diet. Importantly, proteinuria was decreased in the 2K1C+IR group, along with decreased urinary 8-hydroxy-2'-deoxyguanosine excretion and superoxide production of the unclipped kidney. Moreover, the expression of nuclear mineralocorticoid receptor in the unclipped kidney of the 2K1C rats was attenuated by Iron Restriction. These data indicate a novel effect of Iron Restriction on hypertension and renal damage in renovascular hypertension.

  • attenuation of hypertension and renal damage in renovascular hypertensive rats by Iron Restriction
    Hypertension Research, 2016
    Co-Authors: Makiko Oboshi, Yoshiro Naito, Hisashi Sawada, Shinichi Hirotani, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Takeshi Tsujino, Toshiaki Mano, Tohru Masuyama
    Abstract:

    Attenuation of hypertension and renal damage in renovascular hypertensive rats by Iron Restriction

  • Iron is associated with the development of hypoxia-induced pulmonary vascular remodeling in mice.
    Heart and vessels, 2016
    Co-Authors: Yoshiro Naito, Hisashi Sawada, Makiko Oboshi, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Koichi Nishimura, Manami Hosokawa, Yuko Soyama, Shinichi Hirotani
    Abstract:

    Several recent observations provide the association of Iron deficiency with pulmonary hypertension (PH) in human and animal studies. However, it remains completely unknown whether PH leads to Iron deficiency or Iron deficiency enhances the development of PH. In addition, it is obscure whether Iron is associated with the development of pulmonary vascular remodeling in PH. In this study, we investigate the impacts of dietary Iron Restriction on the development of hypoxia-induced pulmonary vascular remodeling in mice. Eight- to ten-week-old male C57BL/6J mice were exposed to chronic hypoxia for 4 weeks. Mice exposed to hypoxia were randomly divided into two groups and were given a normal diet or an Iron-restricted diet. Mice maintained in room air served as normoxic controls. Chronic hypoxia induced pulmonary vascular remodeling, while Iron Restriction led a modest attenuation of this change. In addition, chronic hypoxia exhibited increased RV systolic pressure, which was attenuated by Iron Restriction. Moreover, the increase in RV cardiomyocyte cross-sectional area and RV interstitial fibrosis was observed in mice exposed to chronic hypoxia. In contrast, Iron Restriction suppressed these changes. Consistent with these changes, RV weight to left ventricular + interventricular septum weight ratio was increased in mice exposed to chronic hypoxia, while this increment was inhibited by Iron Restriction. Taken together, these results suggest that Iron is associated with the development of hypoxia-induced pulmonary vascular remodeling in mice.

  • Temporary Dietary Iron Restriction Affects the Process of Thrombus Resolution in a Rat Model of Deep Vein Thrombosis
    PloS one, 2015
    Co-Authors: Makiko Oboshi, Yoshiro Naito, Hisashi Sawada, Shinichi Hirotani, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Daisuke Morisawa, Koichi Nishimura, Kenichi Fujii
    Abstract:

    Background Deep vein thrombosis (DVT) is a major cause of pulmonary thromboembolism and sudden death. Thus, it is important to consider the pathophysiology of DVT. Recently, Iron has been reported to be associated with thrombotic diseases. Hence, in this study, we investigate the effects of dietary Iron Restriction on the process of thrombus resolution in a rat model of DVT.

  • Iron Restriction inhibits renal injury in aldosterone/salt-induced hypertensive mice
    Hypertension Research, 2015
    Co-Authors: Hisashi Sawada, Yoshiro Naito, Makiko Oboshi, Shinichi Hirotani, Toshihiro Iwasaku, Yoshitaka Okuhara, Akiyo Eguchi, Daisuke Morisawa, Tohru Masuyama
    Abstract:

    Excess Iron is associated with the pathogenesis of several renal diseases. Aldosterone is reported to have deleterious effects on the kidney, but there have been no reports of the role of Iron in aldosterone/salt-induced renal injury. Therefore, we investigated the effects of dietary Iron Restriction on the development of hypertension and renal injury in aldosterone/salt-induced hypertensive mice. Ten-week-old male C57BL/6J mice were uninephrectomized and infused with aldosterone for four weeks. These were divided into two groups: one fed a high-salt diet (Aldo) and the other fed a high-salt with Iron-restricted diet (Aldo-IR). Vehicle-infused mice without a uninephrectomy were also divided into two groups: one fed a normal diet (control) and the other fed an Iron-restricted diet (IR) for 4 weeks. As compared with control and IR mice, Aldo mice showed an increase in both systolic blood pressure and urinary albumin/creatinine ratio, but these increases were reduced in the Aldo-IR group. In addition, renal histology revealed that Aldo mice exhibited glomerulosclerosis and tubulointerstitial fibrosis, whereas these changes were attenuated in Aldo-IR mice. Expression of intracellular Iron transport protein transferrin receptor 1 was increased in the renal tubules of Aldo mice compared with control mice. Dietary Iron Restriction attenuated the development of hypertension and renal injury in aldosterone/salt-induced hypertensive mice.